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Gene expression profiling of Human Umbilical Vein Endothelial Cells (HUVEC) after treatment with Erg or control antisense (GeneBloc)

ABSTRACT: The endothelial transcription factor Erg (Ets Related Gene) plays an important role in homeostasis and angiogenesis by regulating many endothelial functions including survival and junction stability. Here we show that Erg regulates endothelial cell migration. Transcriptome profiling of Erg-deficient endothelial cells (EC) identified 80 genes involved in cell migration as candidate Erg targets, including regulators of the Rho GTPases. Inhibition of Erg expression in human umbilical vein endothelial cells (HUVEC) resulted in decreased migration in vitro, whilst Erg over-expression using adenovirus caused increased migration. Live-cell imaging of Erg-deficient HUVEC showed a reduction in lamellipodia, in line with decreased motility. Both actin and tubulin cytoskeletons were disrupted in Erg-deficient EC, with a dramatic increase in tubulin acetylation. Amongst the most significant microarray hit was the cytosolic histone deacetylase (HDAC)-6, a regulator of cell migration. Rescue experiments confirmed that HDAC6 mediates the Erg-dependent regulation of tubulin acetylation and actin localization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE32984 | GEO | 2012/02/27

SECONDARY ACCESSION(S): PRJNA146439

REPOSITORIES: GEO

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Gene expression profiling of Human Umbilical Vein Endothelial Cells (HUVEC) after treatment with Erg or control antisense (GeneBloc)

Project description:The endothelial transcription factor Erg (Ets Related Gene) plays an important role in homeostasis and angiogenesis by regulating many endothelial functions including survival and junction stability. Here we show that Erg regulates endothelial cell migration. Transcriptome profiling of Erg-deficient endothelial cells (EC) identified 80 genes involved in cell migration as candidate Erg targets, including regulators of the Rho GTPases. Inhibition of Erg expression in human umbilical vein endothelial cells (HUVEC) resulted in decreased migration in vitro, whilst Erg over-expression using adenovirus caused increased migration. Live-cell imaging of Erg-deficient HUVEC showed a reduction in lamellipodia, in line with decreased motility. Both actin and tubulin cytoskeletons were disrupted in Erg-deficient EC, with a dramatic increase in tubulin acetylation. Amongst the most significant microarray hit was the cytosolic histone deacetylase (HDAC)-6, a regulator of cell migration. Rescue experiments confirmed that HDAC6 mediates the Erg-dependent regulation of tubulin acetylation and actin localization. The functional role of Erg in EC was studied by gene expressing profiling using three separate HUVEC isolates treated with either control antisense or Erg-specific antisense for 24 or 48 hours.

2012-02-27 | E-GEOD-32984 | biostudies-arrayexpress

Expression data from ERG Si treated and Control HUVEC cells

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ERG activity is regulated by endothelial FAK coupling with TRIM25/USP9x in vascular patterning

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The transcription factor ERG regulates super-enhancers in endothelial cells [ERG siRNA]

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